In the IDD inflammatory microenvironment, CYP1B1 and TNFAIP6 may drive polarisation toward the M1 phenotype via the CCL2/CCR2 axis (Figure S5, Panel B in the Online Supplementary Document), thereby enhancing the release of inflammatory mediators such as IL-1β and IL-6 and inhibiting cartilage matrix synthesis [34]. Here, CCL2 is linked to intervertebral disk degenerative disorder.